ABSTRACT: Myocardial infarction (MI) continues to be a leading cause of death in the United States. Improvements in the diagnosis and treatment of acute MI have reduced in-hospital mortality from 30% in the 1970s to about 5% currently. The traditional functions of hospital pharmacists in MI care involve patient education and counseling on risk-factor modification and drug therapy. However, the introduction of high-sensitivity troponin testing has created uncertainty about optimal drug therapy for post-MI patients. The role of hospital pharmacists in MI care is evolving as new data emerge regarding the standard of care for these patients. Pharmacist interventions are integral to medication optimization, adherence improvement, and individualized patient care to enhance clinical outcomes in MI patients.
Myocardial infarction (MI) remains the leading cause of death in the United States. Annually, approximately 720,000 Americans will have a new coronary event—defined as a first hospitalized MI or sudden cardiac death—and 335,000 will have a recurrent event.1 Improvements in the diagnosis and treatment of acute MI have substantially altered outcomes in these patients. In-hospital mortality from acute MI has declined from approximately 30% in the 1970s to around 5% currently.2 Several drugs have been found to reduce post-MI morbidity and mortality in both acute and long-term management.3 Depending on the presence of specific comorbidities, other drugs may also benefit the post-MI patient.
The traditional role of the hospital pharmacist in the care of MI patients is to educate and counsel the patient about risk-factor modification and drug therapy.4 The pharmacist is also integral in providing resources to help the patient access and remain adherent to post-MI drug therapy. The routine use of high-sensitivity troponin (Tn) testing has led to changes in the epidemiology of MI and created uncertainty about optimal drug therapy in many post-MI patients.5 Accordingly, the hospital pharmacist’s functions are evolving as new data emerge concerning the standard of care for these patients. The objective of this review is to provide an update on the role of the hospital pharmacist in the care of patients with MI.
PATHOPHYSIOLOGY
MI results from a critical imbalance between oxygen supply and demand that leads to cardiac-cell injury and death. In the mid- to late 1970s, it was established that rupture of atherosclerotic plaque in a coronary artery with superimposed thrombus (atherothrombosis) was the most common cause of MI.6 A thrombus that results in total occlusion of an artery causes ST-segment elevation MI (STEMI), whereas non–ST-segment elevation MI (NSTEMI) is associated with subtotal occlusive thrombus. STEMI is a medical emergency wherein the timing of interventions to open the totally occluded artery is crucial for reducing morbidity and mortality.3 In the NSTEMI patient, the timing of medical and procedural interventions varies according to the severity of the patient’s clinical presentation. In NSTEMI patients, clinical status, ECG changes, cardiac imaging, and Tn levels are the primary determinants of the most appropriate therapeutic intervention.
Tn is a protein that is released into the bloodstream when myocardial cells are damaged. High-sensitivity cardiac Tn (hs-cTn) testing is used to detect myocardial injury or MI, with cTn level expressed in ng/L and myocardial injury defined by values exceeding the 99th percentile upper reference limit for healthy adults.5 The advantage of hs-cTn testing is that detection of a normal level enables more rapid ruling out of MI; however, a disadvantage is that elevated hs-cTn level is not specific to the cause of myocardial injury.
Clinical conditions that alter myocardial oxygen supply or demand may be associated with an increase in hs-cTn levels indicative of MI that are not associated with coronary atherothrombosis.7 A condition that produces a critical imbalance of oxygen supply and demand with elevated hs-cTn levels is referred to as demand ischemia. Patients who demonstrate myocardial injury with elevated hs-cTn and underlying atherothrombosis are classified as having type 1 MI, whereas those demonstrating myocardial injury with elevated hs-cTn in the absence of acute atherothrombotic plaque disruption are classified with type 2 MI.8 Type 1 MI comprises both STEMI and NSTEMI, whereas type 2 MI is almost always NSTEMI. Patients with type 2 MI often have underlying coronary artery disease (CAD), but the MI is not associated with underlying coronary atherothrombosis. Diagnosis of type 1 or type 2 MI cannot be conclusively determined without coronary angiography. Therefore, the clinical presentation and other clinical parameters are used to determine the most likely cause of acute MI .
